Disease relevance of Esophagitis, Peptic

• IL1B and IL1RN polymorphic genes and Helicobacter pylori cagA strains decrease the risk of reflux esophagitis [1].
• The role of long-term H2-antagonist therapy in reflux esophagitis is not defined but may be appropriate in scleroderma and Barrett's esophagus [2].
• Epidemiological evidence for a GER/asthma association suggests that about three-fourths of asthmatics, independent of the use of bronchodilators, have acid GER, increased frequency of reflux episodes, or heartburn; and 40% have reflux esophagitis [3].
• We hypothesize that altered expression of cyclin D1 and p53 may be involved in the sequential development of esophageal carcinomas with glandular differentiation induced by the carcinogen, 2,6-dimethylnitrosomorpholine (DMNM) in rats with duodenal content reflux esophagitis [4].
• Clinical studies have shown that proton pump inhibitors, such as omeprazole and lansoprazole, provide more rapid healing and higher healing rates for both duodenal ulcers and reflux esophagitis than do H2-receptor antagonists [5].

Psychiatry related information on Esophagitis, Peptic

• The acute effects of oral metoclopramide (40 mg/day) and domperidone (80 mg/day) on esophageal motor activity and acid reflux were assessed in a randomized, double-blind, placebo-controlled study in 20 patients with erosive reflux esophagitis [6].

High impact information on Esophagitis, Peptic

• We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight) [7].
• For maintenance treatment of reflux esophagitis, omeprazole alone or in combination with cisapride is more effective than ranitidine alone or cisapride alone, and the combination of omeprazole and cisapride is more effective than ranitidine plus cisapride [8].
• Mechanisms of gastroesophageal reflux in patients with reflux esophagitis [9].
• CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection respond significantly better than H. pylori-negative patients to the PPI pantoprazole [10].
• Efficacy of different doses of cimetidine in the treatment of reflux esophagitis. A review of three large, double-blind, controlled trials [11].

Chemical compound and disease context of Esophagitis, Peptic

• Comparison of omeprazole and ranitidine in the treatment of reflux esophagitis [12].
• Sucralfate prevents experimental peptic esophagitis in rabbits [13].
• Oral cimetidine in reflux esophagitis: a double blind controlled trial [14].
• These findings suggest that oral metoclopramide in the dose of 15 mg may be potentially valuable in the management of reflux esophagitis [15].
• Our study indicates that metoclopramide, both parenterally and orally, increased the rate of gastric emptying in those reflux esophagitis patients in whom it was delayed, while bethanechol did not improve the degree of gastric retention in the same patients [16].

Biological context of Esophagitis, Peptic

• Gastric emptying and antral motility in reflux esophagitis. Effect of oral metoclopramide [17].
• The aim of this study was to investigate the effects of cisapride on the triggering and characteristics of secondary peristalsis in patients with reflux esophagitis [18].
• Upper gastrointestinal motility. Part I--The pathophysiologic approach to the management of reflux esophagitis [19].
• AIM: To study the effect of proton pump inhibitor (PPI) treatment on patients with reflux esophagitis and its in vivo effect on apoptosis, p53- and epidermal growth factor receptor (EGFR) expression [20].
• The correlation between radiography, endoscopy, and histology in the diagnosis of reflux esophagitis, as well as the effect of glucagon on double contrast radiography was studied [21].

Anatomical context of Esophagitis, Peptic

• We investigated the acute effect of metoclopramide on lower esophageal sphincter pressure, esophageal contraction amplitude, and gastric emptying and compared metoclopramide, 10 mg four times a day, to placebo in improving the symptoms and objective parameters of reflux esophagitis in 19 patients in a randomized, double-blind 4-wk outpatient trial [22].
• All histopathologic changes in the upper gastrointestinal tract (with the exception of mild reflux esophagitis) reverted to normal following parenteral administration of vitamin B12 [23].
• Higher amounts of PGE2 and NO in the esophageal mucosa of reflux esophagitis patients suggest that similar noxious stimuli trigger the inducible forms of the respective enzyme [24].
• Cimetidine, the first of a new class of pharmacologic agents that dramatically inhibit basal gastric acid secretion, is achieving widespread use for the treatment of such acid peptic disorders as duodenal ulcers, gastritis, and reflux esophagitis [25].
• It has been speculated that impaired salivary flow contributes to abnormal acid clearance of the esophagus in gastroesophageal reflux and results in reflux esophagitis (RE) [26].

Gene context of Esophagitis, Peptic

• Recent studies have shown that IL-8 is likely involved in the development and progression of erosive reflux esophagitis (RE), yet little is known about the two distinct receptors, CXC receptor (CXCR)-1 and -2 [27].
• The rate of secretion of esophageal mucin, EGF and PGE2 under the impact of HC1/pepsin in patients with reflux esophagitis appeared to be significantly impaired, although the basal rate of esophageal PGE2 output remained higher than in controls [28].
• Treatment with rabeprazole almost completely inhibited development of chronic acid reflux esophagitis and significantly decreased expression of cytokines and ICAM-1 mRNA in esophageal tissue compared with control [29].
• Moreover, telomerase activity in esophageal carcinoma was significantly stronger than that in reflux esophagitis and normal epithelium [30].
• Seven patients with cystic fibrosis who had complications of gastroesophageal reflux including abdominal pain, peptic esophagitis, upper gastrointestinal hemorrhage, and esophageal stricture are described [31].

Analytical, diagnostic and therapeutic context of Esophagitis, Peptic

• Four different cimetidine dosage regimens--800 mg u.i.d. HS or nocte, 800 mg u.i.d. dinnertime, 400 mg q.i.d., and 800 mg b.i.d.--were investigated for the treatment of reflux esophagitis in three independent large-scale, double-blind, controlled multicenter trials in which more than 1100 patients participated [11].
• Volume of total mixed saliva and concentration of bicarbonate and N-acetylneuraminic acid during esophageal perfusion with water were higher in patients with reflux esophagitis than in age- and sex-matched controls and were similar to the values found in young healthy volunteers [32].
• Healing and relapse of severe peptic esophagitis after treatment with omeprazole [33].
• The effect of cisapride in patients with reflux esophagitis: an ambulatory esophageal manometry/pH-metry study [34].
• METHODS: In 17 patients with reflux esophagitis and impaired secondary peristalsis cisapride, 10 mg q.i.d., or placebo were administered in a randomized double blind, crossover design for 4 days separated by a 4-7 day washout period [18].

References